Emergencies Resulting from Pulmonary Diseases & Disorders

Emergencies Resulting from Pulmonary Diseases & Disorders
EMS Professions Temple College

Pulmonary Diseases & Disorders
Pulmonary Disease & Conditions may result from: Infectious causes Non-Infectious causes Adversely affect one or more of the following Ventilation Diffusion Perfusion

The Respiratory Emergency may stem from dysfunction or disease of (examples only): Control System Hyperventilation Central Respiratory Depression CVA Thoracic Bellows Chest/Diaphragm Trauma Pickwickian Syndrome Guillian-Barre Syndrome Myasthenia Gravis COPD

The Respiratory Emergency may affect the upper or lower airways Upper Airway Obstruction Tongue Foreign Body Aspiration Angioneurotic Edema Maxillofacial, Larnygotracheal Trauma Croup Epiglottitis

Respiratory Emergencies: Causes
Lower Airway Obstruction Emphysema Chronic Bronchitis Asthma Cystic Fibrosis

The Respiratory Emergency may stem from Gas Exchange Surface Abnormalities Cardiogenic Pulmonary Edema Non-cardiogenic Pulmonary Edema Pneumonia Toxic Gas Inhalation Pulmonary Embolism Drowning

Problems with the Gas Exchange Surface

Pulmonary Edema

Pulmonary Edema: Pathophysiology
A pathophysiologic condition, not a disease Fluid in and around alveoli Interferes with gas exchange Increases work of breathing Two Types Cardiogenic (high pressure) Non-Cardiogenic (high permeability)

Pulmonary Edema High Pressure (cardiogenic)
AMI Chronic HTN Myocarditis High Permeability (non-cardiogenic) Poor perfusion, Shock, Hypoxemia High Altitude, Drowning Inhalation of pulmonary irritants

Cardiogenic Pulmonary Edema: Etiology
Left ventricular failure Valvular heart disease Stenosis Insufficiency Hypertensive crisis (high afterload) Volume overload Increased Pressure in Pulmonary Vascular Bed

Pulmonary Edema High Permeability
Disrupted alveolar-capillary membrane Membrane allows fluid to leak into the interstitial space Widened interstitial space impairs diffusion

Non-Cardiogenic Pulmonary Edema: Etiology
Toxic inhalation Near drowning Liver disease Nutritional deficiencies Lymphomas High altitude pulmonary edema Adult respiratory distress syndrome Increased Permeability of Alveolar-Capillary Walls

Pulmonary Edema: Signs &Symptoms
Dyspnea on exertion Paroxysmal nocturnal dyspnea Orthopnea Noisy, labored breathing Restlessness, anxiety Productive cough (frothy sputum) Rales, wheezing Tachypnea Tachycardia

Management of Non-Cardiogenic Pulmonary Edema
Position Oxygen PPV / Intubation CPAP PEEP IV Access; Minimal fluid administration Treat the underlying cause Diuretics usually not helpful; May be harmful Transport

Adult Respiratory Distress Syndrome
AKA: Non-cardiogenic pulmonary edema A complication of: Severe Trauma / Shock Severe infection / Sepsis Bypass Surgery Multiple blood transfusions Drug overdose Aspiration Decreased compliance Hypoxemia

ARDS Pathophysiology A condition resulting from severe illness or injury and associated with a high mortality rate Increased permeability Pulmonary edema Surfactant destruction Atelectasis Decreased compliance Hypoxemia

ARDS Presentation History Exam Findings
Recent hx of severe illness or injury Often already being treated for underlying cause Exam Findings Dyspnea Evidence of pulmonary edema Poor oxygenation Decreased lung compliance

ARDS Management Airway Management Mechanical Ventilation
Endotracheal intubation Suction Mechanical Ventilation PEEP ECG Monitoring Treat underlying cause May require vasopressors for shock

Pneumonia

Pneumonia Fifth leading cause of death in US
Group of Specific infections Risk factors Cigarette smoking Exposure to cold Extremes of age young old

Pneumonia Inflammation of the bronchioles and alveoli
Products of inflammation (secretions, pus) add to respiration difficulty Gas exchange is impaired Work of breathing increases May lead to Atelectasis Sepsis VQ Mismatch Hypoxemia

Pneumonia: Etiology Viral Bacterial Fungi Protozoa (pneumocystis)
Aspiration

Presentation of Pneumonia
Shortness of breath, Dyspnea Fever, chills Pleuritic Chest Pain, Tachycardia Cough Green/brown sputum May have crackles, rhonchi or wheezing in peripheral lung fields Consolidation Egophony

Management of Pneumonia
Treatment mostly based upon symptoms Oxygen Rarely is intubation required IV Access & Rehydration B2 agonists may be useful Antibiotics (e.g. Rocephin) Antipyretics

Pneumonia: Management
MD follow-up for labs, cultures & Rx Transport considerations Elderly have significant co-morbidity Young have difficulty with oral medications ED vs PMD office/clinic Transport in position of comfort Would an anticholinergic like Atrovent be useful in managing pneumonia?

Pulmonary Embolism

Pulmonary Embolism ~ 50,000 deaths / year ~5% of all sudden deaths
<10% of all PE result in death

Pulmonary Embolism: Pathophysiology
Something moving with flow of blood passes through right heart into pulmonary circulation It reaches an area too narrow to pass through and lodges there Part of pulmonary circulation is blocked Blood: Does not pass alveoli Does not exchange gases

Pulmonary Embolism (PE)
A disorder of perfusion Combination of factors increase probability of occurrence Hypercoagulability Platelet aggregation Deep vein stasis Embolus usually originates in lower extremities or pelvis

Pulmonary Embolism (PE)
Risk factors Venostasis or DVT Recent surgery or trauma Long bone fractures (lower) Oral contraceptives Pregnancy Smoking Cancer

Pulmonary Embolism: Etiology
Most Common Cause = Blood Clots Vessel Wall Injury Virchow’sTriad Hypercoagulability Venous Stasis

Pulmonary Embolism: Etiology
Other causes Air Amniotic fluid Fat particles (long bone fracture) Particulates from substance abuse Venous catheter

Pulmonary Embolism: Signs & Symptoms
Small Emboli Rapid Onset Dyspnea Tachycardia Tachypnea Fever Episodic = Showers Evidence or history of thrombophlebitis Consider early when no other cardiorespiratory diagnosis fits

Larger Emboli Small Emboli S/S plus: Pleuritic pain Pleural rub Coughing Wheezing Hemoptysis (rare)

Very Large Emboli Preceded by S/S of Small & Larger Emboli plus: Central chest pain Distended neck veins Acute right heart failure Shock Cardiac arrest

There are NO assessment findings specific to pulmonary embolism
Pulmonary Embolism: Signs & Symptoms There are NO assessment findings specific to pulmonary embolism

Pulmonary Embolism: Management
Management based on severity of Sx/Sx Airway & Breathing High concentration O2 Consider assisting ventilations Early Intubation Circulation IV, 2 lg bore sites Fluid bolus then TKO; Titrate to BP ~ 90 mm Hg Monitor ECG Rapid transport

PE Management Thrombolytics Rapid transport to appropriate facility
Aspirin & Heparin (questionable if any benefit) Rapid transport to appropriate facility Embolectomy or thrombolytics at hospital (rarely effective in severe cases due to time delay) Poor prognosis when cardiac arrest follows

But the next one they throw might!
Pulmonary Embolism If the patient is alive when you get to them, that embolus isn’t going to kill them. But the next one they throw might!

Pleurisy Inflammation of pleura caused by a friction rub
layers of pleura rubbing together Commonly associated with other respiratory disease

Presentation of Pleurisy
Sharp, sudden and intermittent chest pain with related dyspnea Possibly referred to shoulder May  or  with respiration Pleural “friction rub” may be audible” May have effusion or be dry

Pleurisy Management Based upon severity of presentation
Mostly supportive

Problems with Airway Obstructions

Obstructive Airway Diseases

Obstructive Airway Disease
Asthma Emphysema Chronic Bronchitis

Obstructive Airway Diseases
Asthma experienced by ~ % of US population Mortality rate increasing Factors leading to Obstructive Airway Diseases Smoking Exposure to environmental agents Genetic predisposition How does this differ from “COPD”?

Exacerbation Factors Intrinsic Stress (especially in adults) URI Exercise Extrinsic Cigarette Smoke Allergens Drugs Occupational hazards

General Pathophysiology Specific pathophysiology varies by disease Obstruction in bronchioles Smooth muscle spasm (beta) Mucous accumulation Inflammation Obstruction may be reversible or irreversible

General Pathophysiology Obstruction results in air trapping Bronchioles usually dilate on inspiration Dilation allows air to enter even in presence of “obstruction” Bronchioles tend to constrict on expiration Air becomes trapped distal to obstruction

Lower Airway Disease

Chronic Obstructive Pulmonary Disease
Emphysema Chronic Bronchitis (Rarely Asthma may result in COPD)

COPD: Epidemiology Most common chronic lung disease
14.8 million cases in U.S. 4th leading cause of death 110,000 deaths annually

Emphysema Type A COPD

Emphysema: Definition
Destruction of alveolar walls Distention of pulmonary air spaces Loss of elastic recoil Destruction of gas exchange surface

Emphysema: Incidence Male > females Urban area > rural areas
Age usually > 55

Emphysema:Etiology Smoking Environmental factors
90% of all cases Smokers 10x more likely to die of COPD than non-smokers Environmental factors Alpha – 1 antitrypsin deficiency hereditary 50,000 to 100,000 cases mostly people of northern European descent

Emphysema: Pathophysiology
Decreased surface area leads to decreased gas exchange with blood Loss of pulmonary capillaries & hypercapnia lead to increased resistance to blood flow which leads to pulmonary HTN right heart failure (cor pulmonale)

Emphysema: Pathophysiology
Loss of elastic recoil leads to increased residual volume and CO2 retention Air Trapping Hyperinflation Hypercapnia -> pulmonary vasoconstriction -> V/Q mismatch

Emphysema: Signs and Symptoms
Increasing dyspnea on exertion Non-productive cough Malaise Anorexia, Loss of weight Hypertrophied respiratory accessory muscles

Increased Thoracic AP Diameter (Barrel Chest) Decreased lung/heart sounds Hyperresonant chest

Lip pursing on exhalation Clubbed fingertips Altered blood gases Normal or decreased PaO2 Elevated CO2 Cyanosis occurs LATE in course of disease PINK PUFFER

Chronic Bronchitis Type B COPD

Chronic Bronchitis: Definition
Increased mucus production for > 3 months for > 2 consecutive years Recurrent productive cough

Chronic Bronchitis: Incidence
Males > females Urban areas > rural areas Age usually > 45

Chronic Bronchitis: Etiology
Smoking Environmental irritants

Chronic Bronchitis: Pathophysiology
Mucus plugging/inflammatory edema Increased airflow resistance leads to alveolar hypoventilation Alveolar hypoventilation leads to hypercarbia hypoxemia

Chronic Bronchitis: Pathophysiology
Hypoxemia leads to increased RBC’s w/o oxygen which leads to cyanosis Hypercarbia leads to pulmonary vascular constriction which leads to increased right ventricular work which leads to right heart failure which may progress to cor pulmonale

Chronic Bronchitis: Signs and Symptoms
Increasing dyspnea on exertion Frequent colds of increasing duration Productive cough Weight gain, edema (right heart failure) Rales, rhonchi, wheezing Bluish-red skin color (polycythemia) Headache, drowsiness (increased CO2)

Chronic Bronchitis: Signs and Symptoms
Decreased intellectual ability Personality changes Abnormal blood gases Hypercarbia Hypoxia Cyanosis EARLY in course of disease BLUE BLOATER

COPD Assessment Findings
Chronic condition  acute episode S&S of  work of breathing and/or hypoxemia Use of accessory muscles Increased expiratory effort Tachycardia, AMS, Cyanosis Wheezing, Rhonchi,  LS Thin, red/pink appearance Saturation usually normal in emphysema

COPD: Management Causes of Decompensation
Respiratory infection (increased mucus production) Chest trauma (pain discourages coughing or deep breathing) Sedation (depression of respirations and coughing) Spontaneous pneumothorax Dehydration (causes mucus to dry out)

TRUE HYPOXIC DRIVE IS VERY RARE
COPD: Management Airway and Breathing Sitting position or position of comfort Calm & Reassure Encourage cough Avoid exertion Oxygen Don’t withhold Maintain O2 saturation above 90 % TRUE HYPOXIC DRIVE IS VERY RARE

COPD: Management Ventilation Circulation
Avoid intubation unless absolutely necessary near respiratory failure exhaustion Circulation IV TKO Titrate fluid to degree of dehydration 250 cc trial bolus Excessive fluid may precipitate CHF Monitor ECG

COPD: Management Drug Therapy Obtain thorough medication history
Nebulized Beta 2 agonists Albuterol Terbutaline Metaproterenol Isoetharine

REMEMBER All bronchodilators are potentially arrhythmogenic
COPD: Management REMEMBER All bronchodilators are potentially arrhythmogenic

COPD: Management Drug Therapy Ipratropium (anticholinergic) by SVN
Terbutaline (beta-2 agonist) by MDI, SQ or IV Corticosteroids (anti-inflammatory agent) by IV

COPD: Management Drug Therapy Aminophylline (methylxanthine)
Little evidence of benefit in acute management Is arrhythmogenic Produces toxicity easily 2 to 3 hours to peak effect Magnesium sulfate Also with little supportive evidence Antibiotics

COPD: Management Avoid Sedatives Restlessness = hypoxia Antihistamines
Dry secretions, decrease LOC Epinephrine Myocardial ischemia, arrhythmias Intubation difficult to wean off ventilator

Reversible Obstructive Airway Disease
Asthma

Asthma: Definition Lower airway hyper-responsiveness to a variety of stimuli Diffuse reversible airway obstruction or narrowing Airway inflammation

Asthma: Incidence 50% onset before age 10 33% before age 30
“Asthma” in older patients suggests other obstructive pulmonary diseases Risk Factors Family history of asthma Perinatal exposure to airborne allergens and irritants Genetic hypersensitivity to environmental allergens (Atopy)

Asthma Diagnosis H&P, Spirometry
Hx or presence of episodic symptoms of airflow obstruction airflow obstruction is at least partially reversible alternative diagnoses are excluded

Asthma Commonly misdiagnosed in children as Chronic bronchitis
Recurrent croup Recurrent URI Recurrent pneumonia

Asthma Often triggered by: Exacerbation Cold temperature
Respiratory Infections Vigorous exercise Emotional Stress Environmental allergens or irritants Exacerbation Extrinsic common in children Intrinsic common in adults

Asthma Pathophysiology
Asthma triggered  Bronchial smooth muscle contraction Increased mucus production Bronchial ‘plugging’ Relative dehydration Alveolar hypoventilation  Ventilation Perfusion Mismatch CO2 retention Air ‘Trapping’

Asthma: Pathophysiology
Bronchospasm Bronchial Edema Increased Mucus Production

Cast of airway produced by asthmatic mucus plugs

Difficulty exhaling chest hyperinflation Poor gas exchange hypoxia hypercarbia Increased respiratory water loss dehydration

Asthma: Types Type 1 Extrinsic Classic allergic asthma
Common in children, young adults Seasonal in nature Sudden brief attacks Major component is bronchospasm Good bronchodilator response

Asthma: Types Type 2 Extrinsic Asthma Adults < 35
Long term exposure to irritants More inflammation than Type 1 Extrinsic Does not respond well to bronchodilators Needs treatment with corticosteroids

Asthma: Types Intrinsic Asthma Adult > 35 No immunologic cause
Aspirin sensitivity/nasal polyps Poor bronchodilator response

Asthma: Signs and Symptoms
Onset of attacks associated with “triggers” Dyspnea Non-productive cough Tachypnea Expiratory wheezing Accessory muscle use Retractions

Absence of wheezing IMPENDING RESPIRATORY ARREST!

Tachycardia Pulsus paradoxus in severe attacks Anxiety, restlessness (hypoxia) progressing to drowsiness, confusion (hypercarbia)

Lethargy, confusion, suprasternal retractions RESPIRATORY FAILURE

Early Blood Gas Changes Decreased PaO2 Decreased PaCO2 WHY?

Later Blood Gases Decreased PaO2 Normal PaCO2 IMPENDING RESPIRATORY FAILURE

Still Later Blood Gases Decreased PaO2 Increased PaCO2 RESPIRATORY FAILURE

Asthma: Risk Assessment
Prior ICU admissions Prior intubation >3 ED visits in past year >2 hospital admissions in past year >1 bronchodilator canister used in past month Use of bronchodilators > every 4 hours Chronic use of steroids Progressive symptoms in spite of aggressive Rx

Asthma: Management Airway Breathing
Sitting position or position of comfort Humidified O2 by NRB mask Dry O2 dries mucus, worsens plugs Encourage coughing Consider intubation, assisted ventilation Impending respiratory failure Avoid if at all possible

Asthma: Management Circulation IV TKO Assess for dehydration
Titrate fluid administration to severity of dehydration Trial bolus of 250 cc Monitor ECG, Pulse Oximetry

Asthma: Management Obtain medication history Consider Overdose
Dysrhythmias

Asthma: Management Nebulized Beta-2 agents Nebulized anticholinergics
Albuterol Terbutaline Metaproterenol Isoetharine Nebulized anticholinergics Ipratropium Atropine IV Corticosteroid Methylprednisolone

Asthma: Management Rarely used Magnesium Sulfate (IV) Methylxanthines
Questionable efficacy, Potential Complications Magnesium Sulfate (IV) Methylxanthines Aminophylline (IV)

POSSIBLE BENEFIT IN PATIENTS WITH VENTILATORY FAILURE
Asthma: Management Subcutaneous beta agents Epinephrine 1:1000 q 30 minutes up to 3 doses Adult – 0.3 to 0.5 mg SQ Pediatric – 0.1 to 0.3 mg SQ Terbutaline Adult mg SQ q 30 minutes up to 2 doses Pediatric -SQ or IV infusion usually 0.17 mcg/kg/min POSSIBLE BENEFIT IN PATIENTS WITH VENTILATORY FAILURE

Asthma: Management Use EXTREME caution in giving two sympathomimetics or two doses to same patient Monitor ECG

Asthma: Management Avoid Sedatives Depress respiratory drive
Antihistamines Decrease LOC, dry secretions Aspirin High incidence of allergy

Asthma: Management Continuous Monitoring & Frequent Reassessment
Need for transport? Destination?

Asthma: Management Transport Considerations How severe is the episode?
Is the patient improving? How extensive (invasive) were the required therapies? What does he/she normally do after treatment? Medical Control or PMD consult

Drug Delivery Methods: Review
MDI vs. MDI w/ spacer vs. SVN vs. SQ injection

Asthma unresponsive to beta-2 adrenergic agents
Status Asthmaticus Asthma unresponsive to beta-2 adrenergic agents

Status Asthmaticus Oxygen (humidified if possible)
Nebulized beta-2 agents Nebulized Ipratropium Corticosteroids IV or SQ terbutaline or epinephrine Aminophylline (controversial) Magnesium sulfate (controversial) Intubation Caution with PPV

ALL THAT WHEEZES IS NOT ASTHMA
Golden Rule ALL THAT WHEEZES IS NOT ASTHMA Pulmonary edema Pulmonary embolism Allergic reactions COPD Pneumonia Foreign body aspiration Cystic fibrosis

Lower Airway Disease Cystic Fibrosis

Cystic Fibrosis: Definition
Inherited metabolic disease of exocrine glands and sweat glands Primarily affects digestive, respiratory systems Begins in infancy

Cystic Fibrosis: Etiology
Autosomal recessive gene Both parents must be carriers Incidence Caucasians--1:2000 Blacks--1:17,000 Asians--very rare

Cystic Fibrosis: Pathophysiology
Obstruction of pancreatic, intestinal gland, bile ducts Over-secretion by airway mucus glands mucous plugs Excess loss of sodium chloride in sweat

Cystic Fibrosis: Recognition
History Airway obstruction, chronic cough Recurrent respiratory infections May be oxygen-dependent Diffuse Wheezing Frequent, foul-smelling stools Salty taste on skin Intolerance of hot environments

Cystic Fibrosis: Management
Position of comfort Oxygen Suctioning Nebulized Beta agonists May not be very helpful but worth attempting if absence of contraindications Assisted ventilation

Lower Airway Disease Neoplasms of the Lung

Neoplasms of the Lung 150,000 cases
Usually occurs between ages of 55 and 65 Most die within one year 20% only local lung involved 25% spread to lymphatic system 55% result in distant metastatic cancer

Neoplasms of the Lung Prevention
Centered on prevention of smoking in youths Then, cessation in current smokers Avoid environmental hazards (e.g. asbestos)

Neoplasms of the Lung Presentation
Respiratory Difficulty progressing to Distress Cough, Hemoptysis Hoarseness or voice change Dysphagia

Management of Neoplasms of the Lung
Supportive care based upon presentation Oxygen Consider presence of advance directives or DNR Patient’s wishes Family discussions MD prognosis If appropriate Assist ventilations or Intubate IV access & rehydration Bronchodilators Analgesia for pain (small, slow doses)

Hyperventilation Syndrome

Brady Textbook Correction, Vol. 3, p. 57 Table 1-4: These are NOT Causes of hyperventilation syndrome A diagnosis of EXCLUSION!!! An increased ventilatory rate that DOES NOT have a pathologic origin Results from anxiety Remains a real problem for the patient

Hyperventilation Syndrome: Pathophysiology
Tachypnea or hyperpnea secondary to anxiety Decreased PaCO2 Respiratory alkalosis Vasoconstriction Hypocalcemia Decreased O2 Release to Tissues

Hyperventilation Syndrome: Signs & Symptoms
Light-headedness, giddiness, anxiety Numbness, paresthesias of: Hands Feet Circumoral area Cold hands, feet Carpopedal spasms Dyspnea Chest pain

Hyperventilation Syndrome: Signs & Symptoms
Rapid breathing Cool & possibly pale skin Carpopedal spasm Dysrhythmias Sinus Tachycardia SVT Sinus arrhythmia Loss of consciousness and seizures (late & rare)

Hyperventilation Syndrome: Management
Thorough assessment to rule out physiologic causes Rule out head injury, metabolic acidosis Metabolic acidosis and increased ICP can cause rapid breathing that mimics hyperventilation syndrome!

Oxygen based upon presentation Reassurance & Patience Coach breathing rate CAUTION: Rebreathing into bag or NRB Monitoring ECG Pulse oximetry

Educate patient & family Consider possible psychopathology especially in “repeat customers” Transport occasionally required If loss of consciousness, carpopedal spasm, muscle twitching, or seizures occur: Monitor EKG IV TKO Transport

Serious diseases can mimic hyperventilation Hyperventilation itself can be serious

Pulmonary Infectious Diseases

Laryngotracheobronchitis (Croup)
Common syndrome of infectious upper airway obstruction Viral infection parainfluenza virus Subglottic Edema larynx, trachea, mainstem bronchi Usually 3 months to 4 years of age

Croup: Signs & Symptoms
Gradual onset (several days) Often begins with Sx of URI May begin with only low grade fever Hoarseness Cough “Seal Bark Cough” “Brassy Cough” Nocturnal episodes of increased dyspnea and stridor

Croup: Signs & Symptoms
Evidence of respiratory distress Tracheal tugging Substernal/intercostal retractions Accessory muscle use Inspiratory stridor or respiratory distress may develop slowly or acutely

Croup: Management Usually requires little out of home treatment
Calm & Prevent agitation!!! Moist cool air - mist Humidified O2 by mask or blowby Do Not Examine Upper Airways!!!

Croup: Management If in respiratory distress:
Racemic epinephrine via nebulizer Decreases subglottic edema (temporarily) Necessitates transport for observation for rebound IV TKO - ONLY if severe respiratory distress Transport

Bronchiolitis Pathophysiology
Viral Disease resulting in inflammation of the lower airways Usually caused by RSV Typically affects children months old (15% of all children < 2 years old) Usually occurs in the winter or early spring

Bronchiolitis: Presentation
Usually less than 18 months during the winter or early spring wheezing mild to moderate respiratory difficulty no asthma history associated with other viral symptoms runny nose sneezing cough low grade fever

Bronchiolitis: Management
Usually require little out of home treatment Oxygen, mask or blowby Nebulized Bronchodilators if respiratory distress May not respond well or at all Transport

Epiglottitis Bacterial infection (Hemophilus influenza )
Edema of epiglottis (supraglottic) partial upper airway obstruction Typically affects 3-7 year olds

Epiglottitis: Presentation
Age: 3-7 years of age can occur in adults can occur in infants Rapid onset & progression Fever Severe sore throat Dysphagia Muffled voice Drooling

Epiglottitis: Presentation
Respiratory difficulty Stridor Usually in an upright, sitting, tripod position Child may go to bed asymptomatic and awaken during the night with sore throat painful swallowing respiratory difficulty

Epiglottitis: Management
Immediate life threat (8-12% die from airway obstruction) Do NOT attempt to visualize airway Allow child to assume position of comfort AVOID agitation of the child!!! AVOID anxiety of the healthcare providers!!! O2 by high concentration mask

Epiglottitis: Management
If respiratory failure is eminent: IV TKO ONLY if eminent or respiratory arrest Be prepared to take control of airway Intubation equipment with smaller sized tubes Needle cricothyrotomy & jet ventilation equipment Rapid but calm transport Appropriate facility

Upper Respiratory Infection
Common illness Rarely life-threatening Often exacerbates underlying pulmonary conditions May become more significant in some patients Immunosuppressed Elderly Chronic pulmonary disease

Upper Respiratory Infection
Prevention Avoidance is nearly impossible Too many potential causes Temporarily impaired immune system Best prevention strategy is handwashing Covering of mouth during sneezing and coughing also helpful

Pathophysiology of URI
Wide variety of bacteria and viruses are causes Normal immune system response results in presentation 20-30% are Group A streptococci Most are self-limiting diseases

Presentation of URI Symptoms Signs Sore throat Fever Chills HA
Cervical adenopathy Erythematous pharynx Positive throat culture (bacterial)

Management of URI Usually requires no intervention
Oxygen if underlying condition has been exacerbated Rarely, pharmacologic interventions are required Bronchodilators Corticosteroid Occasionally, transport required Key question: Destination?

Central Respiratory Depression

Respiratory Depression: Causes
Head trauma CVA Depressant drug toxicity Narcotics Barbiturates Benzodiazepines ETOH

Respiratory Depression: Recognition
Decreased respiratory rate (< 12/min) Decreased tidal volume Decreased LOC Use Your Stethoscope Look, Listen, Feel THEY PROBABLY AREN’T If you can’t tell whether a patient is breathing adequately...

Respiratory Depression: Management
Airway Open, clear, maintain Consider endotracheal intubation The need to VENTILATE is not the same as the need to INTUBATE

Breathing Oxygenate, ventilate Restore normal rate, tidal volume Oxygen alone is INSUFFICIENT if Ventilation is INADEQUATE

Circulation Obtain vascular access Monitor EKG (Silent MI may present as CVA) Manage Cause Check Blood Sugar Consider Narcan 2mg IV push if S/S suggest narcotic overdose Intubate if can not find or treat cause

Thoracic Bellows Malfunction
Pickwickian Syndrome Guillian-Barre Syndrome Myasthenia Gravis

Pickwickian Syndrome Results from extreme obesity
form of sleep apnea Decreased excursion of chest wall, diaphragm causes hypoventilation CO2 retention

Pickwickian Syndrome Signs and Symptoms Treat symptomatically Headache
Drowsiness Inappropriate sleepiness Sleep apnea Treat symptomatically Assist ventilations as needed

Guillian-Barre´ Syndrome
Autoimmune disease Leads to inflammation and degeneration of sensory and motor nerve roots (de-myelination) Progressive ascending paralysis Progressive tingling and weakness Moves from extremities then proximally May lead to respiratory paralysis (25%)

Guillian-Barre´ Syndrome
Self-Limiting Recovery is spontaneous and complete in 95% of cases In good outcomes, symptoms clear in 15 to 20 days Often takes weeks or months

Guillian-Barre´ Syndrome Management
Treatment based on severity of symptoms Control airway Support ventilation Oxygen Transport in cases of respiratory depression, distress or arrest

Myasthenia Gravis Autoimmune disease
Causes loss of ACh receptors at neuromuscular junction Attacks the ACh transport mechanism at the NMJ Episodes of extreme skeletal muscle weakness Can cause loss of control of airway, respiratory paralysis

Myasthenia Gravis Presentation
Gradual onset of muscle weakness Face and throat Extreme muscle weakness Respiratory weakness -> paralysis Inability to process mucus

Myasthenia Gravis Management
Treat symptomatically Watch for aspiration May require assisted ventilations Assess for Pulmonary infection Transport based upon severity of presentation

Other Causes of Respiratory Emergencies

Angioneurotic Edema Allergic reaction Common Causes
Edema of tongue, pharynx, larynx NOT the SAME as anaphylaxis Common Causes Food (seafood or nuts) Drugs (penicillin or sulfa) Hymenoptera sting (ants, bees, wasps)

Angioneurotic Edema Signs and Symptoms Itching in palate
“Lump in throat” Hoarseness Stridor Coughing Dyspnea Urticaria (hives)

Angioneurotic Edema: Management
Based upon severity of presentation Establish airway O2 via NRB IV lg bore TKO Epinephrine 1: mg SQ repeat after 20 minutes if needed

Angioneurotic Edema: Management
Based upon severity of presentation (cont) Diphenhydramine 25 to 50mg IM/IV In severe cases, Consider Positive pressure ventilation Endotracheal intubation Surgical airway

Spontaneous Pneumothorax
Low incidence Many are well tolerated Risk Factors Males Younger age Thin body mass Marfan’s syndrome History of Obstructive Airway Disease

Presentation of Spontaneous Pneumothorax
Symptoms Sudden SOB Sudden pleuritic CP Signs Mild pallor, tachycardia, tachypnea Decreased lung sounds usually very localized Increasing pneumothorax presents with more severe S/S

Management of Simple Pneumothorax
Oxygen based on severity of S/S Assisted ventilation and intubation as needed May worsen pneumothorax Rarely needed IV access if severe symptoms are present Position of comfort Transport

Case Studies

What would you like to include in your initial differential diagnosis?
Case One It is 1430 hrs. You are called to a business for a “possible stroke.” The patient is a 20-year-old female complaining of dizziness and of numbness around her mouth and fingertips. What would you like to include in your initial differential diagnosis?

What therapies, if any, would you like to begin?
Case One Initial Assessment Airway: Open, maintained by patient Breathing: Rapid, deep, regular; no accessory muscle use or retractions Circulation: Radial pulses present, rapid, full; Skin warm, dry; capillary refill < 2 seconds Disability: Awake, alert, anxious What therapies, if any, would you like to begin?

Would you like to make any Changes to your therapies or Diff Dx?
Case One Vital Signs P: 126 strong, regular R: 26 deep, regular BP: 130/82 Physical Exam Chest: BS present, equal bilaterally; no adventitious sounds Extremities: Equal movement in all extremities; no weakness; hands cool Oxygen saturation: 98% Would you like to make any Changes to your therapies or Diff Dx?

Case One History Allergies: NKA Medications: Birth control pills
Past History: No significant past history; no history of smoking Last Meal: Lunch 2 hours ago Events: S/S began suddenly after argument with supervisor

Case One What problem do you now suspect?
How would you manage this patient?

What would you like to include in your differential diagnosis?
Case Two It is 0530 hours. You are called to a residence to see a child with “a very high fever and difficulty breathing.” The patient is a 6-old-female. Mother says the child woke up crying about 2 hours ago. What would you like to include in your differential diagnosis?

What therapies, if any, would you like to begin now?
Case Two Initial Assessment Airway: Inspiratory stridor audible Breathing: Rapid, shallow, labored Circulation: Radial pulses present, rapid, weak; skin pale, hot, diaphoretic; capillary refill is 2 seconds Disability: Awake, alert, obviously frightened and in acute distress What therapies, if any, would you like to begin now?

Would you like to make any Changes to your therapies or Diff Dx?
Case Two Vital Signs P: 130 weak, regular R: 32 shallow, regular with stridor BP: 110/70 Physical Exam HEENT: Flaring of nostrils; accessory muscle use on inspiration; drooling present Chest: BS present, equal bilaterally; no adventitious sounds Oxygen saturation: 92% Would you like to make any Changes to your therapies or Diff Dx?

Case Two History Allergies: NKA Medications: None
Past History: No significant past history Last Meal: Dinner at about 1800 hours Events: Awakened with severe sore throat. Has experienced increasing difficulty breathing. Will not eat or drink. Says it hurts to swallow

Case Two What problem do you now suspect?

How narrow a Differential Diagnosis can you compile at this point?
Case Three At 2330 hrs you are called to a residence to see a child with “difficulty breathing.” The patient is a 3 year old male. How narrow a Differential Diagnosis can you compile at this point?

Case Three Initial Assessment
Airway: Open, maintained by patient, mild stridor audible Breathing: Rapid, shallow, labored Circulation: Radial pulses present, weak, regular; Skin pale, warm, moist; Capillary refill <2 seconds Disability: Awake, sitting up in bed, looks tired and miserable

Now you can narrow your Diff Dx? To what?
Case Three Vital Signs P: 100 weak, regular R: 30 shallow, labored with stridor BP: 90/50 Physical Exam HEENT: Use of accessory muscles present; no drooling Chest: BS present, equal bilaterally with no adventitious sounds. Auscultation difficult because of stridor and barking cough Now you can narrow your Diff Dx? To what?

Case Three History Allergies: NKA
Medication: Tylenol for fever before bedtime Past history: No significant past history Last meal: Dinner around 1800 hours Events: Patient has had “cold” for about 3 days. Reasonably well during day. Awakens around midnight with high-pitched cough that sounds like a dog barking

Case Three What problem do you suspect?

What is your differential diagnosis?
Case Four At 1945 hours you are dispatched to a “breathing difficulty” at Long John Silver’s. The patient is a 26-year-old female complaining of strange feeling in her mouth and difficulty swallowing. What is your differential diagnosis?

Case Four Initial Assessment
Airway: Open, maintained by patient, difficulty swallowing, voice is hoarse Breathing: Rapid, labored Circulation: Radial pulses present, strong, regular; Skin “flushed”; Capillary refill < 2 seconds Disability: Awake, alert, very anxious

What therapies do you want to initiate?
Case Four Vital Signs P: 120 strong, regular R: 26 regular, slightly labored BP: 118/90 Physical Exam HEENT: Puffiness around eyes; Lips appear swollen; Mild accessory muscle use Chest: BS present, equal bilaterally; No adventitious sounds Urticaria on upper chest, extremities Oxygen saturation: 94% What therapies do you want to initiate?

Case Four History Allergies: No drug allergies; Has experienced itching previously when eating shrimp Medications: None Past history: No significant past history; no history of smoking Last meal: In progress at time of call Events: Began to experience itching and difficulty swallowing after eating “fish and chips”

Case Four What problem do you suspect?
How would you manage this patient? The patient begins to have increased difficulty swallowing, increased anxiety, and increased difficulty breathing. What do you want to do now?

Case Five At 0130 you are dispatched to an “unconscious person--police on location.” The patient is a 27-year-old male who is apparently unconscious. The police report they found him lying in an alleyway while they were on routine patrol. He is known to live “on the streets”.

What therapies would you like to begin?
Case Five Initial Assessment Airway: Controllable with manual positioning Breathing: Very slow, shallow Circulation: Radial pulses present, weak; Skin pale, cool, moist; Capillary refill 3 seconds Disability: Unconscious, unresponsive to painful stimuli What therapies would you like to begin?

Case Five Vital Signs Physical Exam P: 70 regular, weak
R: 4 shallow, regular; alcohol odor on breath BP: 100/70 Physical Exam HEENT: Pupils pinpoint, non-reactive Chest: BS present, equal bilaterally Abdomen: Soft, non-tender Extremities: Needle tracks present Blood glucose: 40 mg/dl

Case Five What problem or problems do you suspect?

Emergencies Resulting from Pulmonary Diseases & Disorders

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Emergencies Resulting from Pulmonary Diseases & Disorders

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